This document discusses virilization and hirsutism. It defines virilization as clinical features associated with high male hormones in women, such as hirsutism, acne, deepening of voice, increased muscle mass and breast atrophy. Hirsutism is specifically defined as excessive hair growth in a male pattern in women. Potential causes of hirsutism include polycystic ovarian syndrome, congenital adrenal hyperplasia, exogenous androgen use, and androgen-secreting tumors. The document provides details on evaluating potential causes and treating hirsutism.

1. Virilization

2. Virilization
Clinical features associated with a high level of
male hormones in women.
• Hirsuitism
• Acne
• Deepening of voice
• Increased muscle mass
• Breast atrophy

3. Hirsutism
• Excessive growth of thick terminal hair in a male
distribution in women (upper lip, chin, chest, back,
lower abdomen, thigh, forearm)
• Most common presentation of endocrine disease.
• DD: Hypertrichosis, which is generalised excessive
growth of vellus hair.
• The aetiology is androgen excess

4. Androgens and Hirsuitism
• Hirsutism can be caused by either an
increased level of androgens or an
oversensitivity of hair follicles to androgens.
• Testosterone stimulates hair growth, (size,
intensity of growth and pigmentation).

5. obesity/insulin and Hirsuitism
• High circulating levels of insulin are implicated in
women for the development of hirsutism.
• Obese (insulin resistant hyperinsulinemic)
women are at high risk of becoming hirsute.
• Treatments that lower insulin levels lead to a
reduction in hirsutism.
• High concentration of insulin (directly and
through IGF I) is thought to stimulate theca cells
in ovaries to produce androgens.

6. Hirsuitism: Causes
• Idiopathic
• Polycystic ovarian syndrome
• Congenital adrenal hyperplasia
• Exogenous androgen administration
• Androgen-secreting tumour of ovary or
adrenal cortex

7. Hirsuitism: Idiopathic
• Often familial
Mediterranean or Asian background
• Investigations: normal
• Treatment:
–Cosmetic measures
–Anti-androgens

8. Hirsuitism: PCOS
• Aetiology -poorly understood
• Constellation of clinical and biochemical
features of varying severity
–Obesity
–Oligomenorrhoea/ Secondary amenorrhoea
–Infertility
–multiple cysts in the ovaries

9. Hirsuitism: PCOS
Mechanisms* Manifestations
Pituitary dysfunction High serum LH
High serum prolactin
Anovulatory menstrual
cycles
Oligomenorrhoea
Secondary amenorrhoea
Cystic ovaries
Infertility
Androgen excess Hirsutism
Acne
Obesity Hyperglycaemia
Elevated oestrogens
Insulin resistance Dyslipidaemia
Hypertension

10. Hirsuitism: PCOS
• Investigations:
LH:FSH ratio > 2.5:1
Minor elevation of androgens
Mild hyperprolactinaemia
• Treatment
Weight loss
Cosmetic measures
Anti-androgens
Insulin-sensitising drugs

11. Hirsuitism: Congenital adrenal hyperplasia
• 95% 21-hydroxylase deficiency
• Clinical Features:
–Pigmentation
–History of salt-wasting in childhood
–Ambiguous genitalia
–Adrenal crisis when stressed

14. Hirsuitism: Congenital adrenal hyperplasia
• Investigations
– Elevated androgens, suppressible with
dexamethasone
–Abnormal rise in 17OH-progesterone with ACTH
• Treatment
–Glucocorticoid replacement administered in
reverse rhythm to suppress early morning ACTH

15. Hirsuitism: Exogenous androgens
• Athletes
Virilised
• Investigations:
–Low LH and FSH
–Analysis of urinary androgens may detect
drug of misuse
• Treatment:
–Stop steroid misuse

16. Hirsuitism: Androgen-secreting tumour ovary or
adrenal cortex
• Rapid onset virilisation:
–clitoromegaly
–deep voice
–balding
–breast atrophy

17. Hirsuitism: Androgen-secreting tumour ovary or
adrenal cortex
• Investigations:
– High androgens which do not suppress with
dexamethasone or oestrogen
– Low LH and FSH
– CT or MRI usually demonstrates a tumour
• Treatment:
– Surgical excision

18. Hirsuitism : Clinical approach
• The severity of hirsutism is subjective
• Important observations are –
– Drug and menstrual history
– Calculation of BMI
– Measurement of BP
– Examination for virilisation (clitoromegaly, deep
voice, male-pattern balding, breast atrophy)
– Acne vulgaris
– Cushing's syndrome
• When recent & with virilisation, suggestive of a
rare androgen-secreting tumour

19. Hirsuitism:Investigations
Random blood sampling for testosterone,
prolactin, LH and FSH

20. Hirsuitism:Investigations
• Random blood – testosterone, Prl, LH and FSH.
• If Cushingoid features +: Overnight 1 mg Dexa
suppression test

21. Hirsuitism:Investigations
• Random blood – testosterone, Prl , LH and FSH.
• If Cushingoid : Overnight 1 mg DST
• If testosterone levels are high (with low LH &
FSH): look for source of excess androgen

22. Hirsuitism:Investigations
• Random blood – testosterone, Prl , LH and FSH.
• If Cushingoid : Overnight 1 mg DST
• If testosterone high (with low LH & FSH): ? source
• Suspected CAH (21-hydroxylase deficiency): short
ACTH stimulation test, with measurement of
17OH-progesterone

23. Hirsuitism: Investigations
• Androgen-secreting tumours: Testosterone is
not suppressible by
–Dexamethasone
• Overnight or
• 48-hour low-dose suppression test
–Oestrogen (30 μg / day X 7 days)
• CT or MRI of the adrenals and ovaries

24. Hirsuitism: Treatment
• Cosmetic measures - shaving, bleaching and
waxing
• Electrolysis and laser treatment : for small areas
• Eflornithine cream : Inhibits ornithine
decarboxylase in hair follicles & may reduce hair
growth

25. Hirsuitism: Treatment
• Weight reduction for obese patients with PCOS
–enhances insulin sensitivity
–reduces the peripheral conversion of androgens
by adipose tissue
–reduces metabolic clearance of cortisol, thereby
reducing ACTH-dependent adrenal androgen
secretion

26. Hirsuitism: Treatment
If these conservative measures have failed-
• Anti-androgen therapy
The life cycle of hair follicles is at least 3 months,
so no improvement is likely before this. Only
replacement hair growth is suppressed.
• Insulin-sensitising drugs (thiazolidinediones and
biguanides)
Have a role but unless the patient has lost
weight, the hirsutism will return once
discontinued.

27. ANTI-ANDROGEN THERAPY
• Androgen receptor antagonists
–Cyproterone acetate
–Spironolactone
• 5 α-reductase inhibitors (prevents conversion of
testosterone to active form)-
–Finasteride
• Suppress ovarian steroid production and elevate
SHBG (sex hormone-binding globulin )
– Oestrogen (+ Cyproterone acetate)
• Suppress adrenal androgen production-
–Glucocorticoids